Goa is involved in several C. elegans behaviors such as egg-laying, movement and feeding (Mendel et al., 1995 and Ségalat et al., 1995). We isolated 24 independent mutations that revert the phenotype of syIs17 ( a Goa gain-of-function transgenic integrant under the control of a heat shock promoter). These define 8 complementation groups named sags (Suppressors of Activated Goa). Two of the complemetation groups,
sag-1 and
sag-2, appear to act in Goa signaling based on several experiments. Animals deficient in either gene are hyperactive, egg-laying constitutive and have empty uteri; as do
goa-1 loss-of-function mutants. Western blot analysis indicates that heat-shock induced GOA-1 is not affected in
sag-1 and
sag-2 strains and thus these mutations likely affect Goa signaling rather than its synthesis.
sag-1 and
sag-2 also suppress syIs9, an integrated strain with activated Goa under its own promoter, indicating that they act in cells that normally express GOA-1.
sag-1 is allelic to
dgk-1 which encodes a Diacylglycerol Kinase (Nurrish et al., page 44, 1997 international C. elegans meeting). We have positionally cloned
sag-2 and find that it encodes a RGS protein (Regulators of G protein Signaling), raising the possibility that RGS proteins act as effectors as well as regulators of G proteins. SAG-2 might also act as an effector of GOA-1 that inhibits signaling by another Ga subunit.